There are many causes of chest pain. Non-cardiac conditions can mimic a myocardial infarction, and so the ECG can be extremely useful when making a diagnosis. However, as always, the ECG should always be interpreted in its clinical context. The history (including an assessment of coronary risk factors), to a lesser extent the physical examination and other tests including biomarkers of myocardial necrosis, are key to an accurate diagnosis and risk stratification. Some causes of chest pain are listed in Box 6.1. The ECG in Fig. 6.1 was recorded in an accident and emergency (A&E) department from a 44-year-old man with rather vague chest pain. He was thought to have a viral illness and his ECG was considered to be within normal limits. He was allowed to go home, and died later that day. The post-mortem examination showed a myocardial infarction which was probably a few hours old, and corresponded with his A&E attendance. The features of acute chest pain associated with different causes are summarized in Box 6.2. The physical examination of a patient with chest pain may reveal nothing other than the signs associated with the pain itself (anxiety, sinus tachycardia, restlessness or a cold and sweaty skin), but some specific signs are worth looking for: Remember that the ECG can be normal, especially in the early stages of a myocardial infarction. Having said that: Myocardial infarction is, properly, a term describing myocardial cell death due to ischaemia. The histological changes – and ECG changes – can take several hours to appear, and the entire process leading to a healed infarction can take 5 or 6 weeks. Serial ECGs are therefore an important part of the assessment of patients with chest pain. Myocardial injury causes release into the blood of biomarkers including troponin T or I and the MB fraction of creatine kinase (CK-MB). Blood samples should be taken immediately to measure appropriate biomarkers, usually with a high sensitivity troponin assay. However, it is important to remember that plasma biomarker levels take time to rise and the optimal timing of measurements taken to exclude a coronary event depends on the assay used (check with your local laboratory). Therefore, the release of troponin can reflect the necrosis of myocardial cells; however, it also occurs in situations other than coronary artery occlusion (Box 6.3). Thus, although a rise in the blood levels of troponin supports the diagnosis of myocardial infarction, it is not sufficient, and the most commonly used parts of the ‘universal definition’ of myocardial infarction require both clinical evidence of myocardial ischaemia and a rise and/or fall of blood troponin levels. Box 6.4 shows the types of infarction listed in the universal definition, drawn up by the ESC/ACCF/AHA/WHF Task Force.* Acute coronary syndromes are subdivided into those with and without ST segment elevation (ST elevation myocardial infarction [STEMI] and non-ST elevation myocardial infarction [NSTEMI]. These are also referred to sometimes as STE segment elevation ACS (STE-ACS) and non ST segment elevation ACS (NSTE-ACS). The majority of STEMI and some NSTEMI patients develop a rise in troponin, but this may be prevented by very early intervention. Patients with a NSTEMI whose troponin remains normal are classified as having unstable angina. To be as simple as possible, and to avoid confusion, throughout this book we will only describe the relevant ECGs as showing a STEMI or a NSTEMI.‘Stable angina’ is an entirely proper diagnostic label for a patient with intermittent chest pain, often on exertion, associated with transient ‘ischaemic’ ECG changes, and ‘chest pain of unknown cause’ is the best label if no diagnosis has been made. All patients with STEMI should be considered for primary angioplasty or urgent reperfusion therapy where timely percutaneous coronary intervention is not available and should be treated with guideline-recommended medical therapies. The sequence of features characteristic of STEMI is: The universal definition of STEMI requires new ST segment elevation at the J point (the junction of the S wave and the ST segment) in two contiguous leads, with the cut-off points in leads V2–V3 at > 0.2 mV in men or > 0.15 mV in women, and in other leads at > 0.1 mV. The ECG leads that show the changes typical of a myocardial infarction depend on the part of the heart affected. Figs 6.2–6.4 show traces taken from a patient with a typical history of myocardial infarction: on admission to hospital, 3 h later, and 2 days later. The main changes are in the inferior leads: II, III and VF. Here the ST segments are initially raised, but then Q waves appear and the T waves become inverted. Fig. 6.2 includes coronary angiograms and a cardiac magnetic resonance imaging (MRI) showing the myocardial injury resulting from an occluded right coronary artery in an inferior STEMI. The changes of anterior infarction are seen in leads V2–V5. Lead V1, which lies over the right ventricle, is seldom affected (see Fig. 6.5, which includes corresponding coronary angiograms and cardiac MRI). When the lateral wall of the left ventricle is damaged by occlusion of the left circumflex coronary artery, leads I, VL and V6 will show infarction changes. Fig. 6.6 shows the record of a patient with an acute lateral STEMI, with the corresponding coronary angiograms and cardiac MRI. Fig. 6.7 shows a record taken 3 days after a lateral infarction, with Q waves and inverted T waves in leads I, VL and V6. The ECG in Fig. 6.8 shows an acute STEMI affecting both the anterior and lateral parts of the left ventricle. The ECG in Fig. 6.9 was recorded several weeks after an anterolateral myocardial infarction. Although the changes in leads I and VL appear ‘old’, having an isoelectric ST segment, there is still ST segment elevation in leads V3–V5. If the patient had just been admitted to hospital with chest pain these changes would be taken to indicate an acute infarction, but this patient had pain more than a month previously. Persistent ST segment elevation is quite common after an anterior infarction: it sometimes indicates the development of a left ventricular aneurysm, but it is not reliable evidence of this. An old anterior infarction often causes only what is called ‘poor R wave progression’. Fig. 6.10 shows the record from a patient who had had an anterior infarction some years previously. A normal ECG would show a progressive increase in the size of the R wave from lead V1 to V5 or V6 (see p. 19). In this case, the R wave remains very small in leads V3 and V4, but becomes normal-sized in V5. This loss of R-wave ‘progression’ indicates the old infarction. The time taken for the various ECG changes of infarction to occur is extremely variable, and the ECG is an unreliable way of deciding when an infarction occurred. Serial records showing progressive changes are the only way of timing the infarction from the ECG. It is possible to ‘look at’ the back of the heart by placing the V lead on the back of the left side of the chest, but this is not done routinely because it is inconvenient, and the complexes recorded are often small. An infarction of the posterior wall of the left ventricle can, however, be detected from the ordinary 12-lead ECG because it causes a dominant R wave in lead V1. Normally the left ventricle, being more muscular than the right, exerts a greater influence on the ECG, so in lead V1 the QRS complex is predominantly downward. With a posterior infarction, the rearward-moving electrical forces are lost, so lead V1 ‘sees’ the unopposed forward-moving depolarization of the right ventricle, and records a predominantly upright QRS complex. Fig. 6.11 shows the first record from a patient with acute chest pain. There is a dominant R wave in lead V1 and ischaemic ST segment depression in leads V2–V4. The chest electrodes were then moved to the V7–V9 positions: all in the same horizontal plane as V5, with V7 on the posterior axillary line, V9 at the edge of the spine, and V8 halfway between, on the midscapular line. The ECG record then showed raised ST segments, with Q waves typical of an acute infarction. Inferior infarction is sometimes associated with infarction of the right ventricle. Clinically, this is suspected in a patient with an inferior infarction when the lungs are clear but the jugular venous pressure is elevated. The ECG will show raised ST segments in leads recorded from the right side of the heart. The positions of the leads correspond to those on the left side as follows: V1R is in the normal V2 position; V2R is in the normal Vi position; V3R, etc. are on the right side, in positions corresponding to V3, etc. on the left side. Fig. 6.12 is from a patient with an acute right ventricular infarct. Note
The ECG in patients with chest pain
History and examination
Acute chest pain
The ECG in the presence of acute chest pain
The ECG in patients with myocardial ischaemia
ECG changes in STEMI
Inferior infarction
Anterior and lateral infarction
Posterior infarction
Right ventricular infarction
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
The ECG in patients with chest pain
6
Inverted T wave in lead III
Flattened T wave in lead VF
Fig. 6.1
Raised ST segments in leads III and VF
Angiogram showing normal right coronary artery
Angiogram showing occluded right coronary artery in inferior STEMI
MRI showing established inferior myocardial infarction (white area – arrowed)
Fig. 6.2
Deeper Q waves in leads III and VF
Fig. 6.3
Q waves, normal ST segments, and inverted T waves in leads III and VF
Fig. 6.4
Raised ST segment in lead V2
MRI showing established antero-apical myocardial infarction (white area – arrowed)
Angiogram showing normal left coronary artery: LMS, left main stem coronary artery; Cx, circumflex branch; LAD, left anterior descending branch
Angiogram showing occluded left anterior descending branch in anterior STEMI
Fig. 6.5
Raised ST segments in leads I and VL STEMI
MRI showing established lateral myocardial infarction (white area – arrowed)
Angiogram showing normal left coronary artery: LMS, left main stem coronary artery; CX, circumflex branch; LAD, left anterior descending branch
Angiogram showing occluded left circumflex branch in lateral STEMI
Fig. 6.6
Inverted T waves in leads I and VL
Fig. 6.7
S waves in leads II and III: left axis deviation
Fig. 6.8
Raised ST segment in lead V3
Fig. 6.9
Small R wave in lead V4
Tall R wave in lead V5
Fig. 6.10
Dominant R wave in lead V1
Q wave and raised ST segment in lead V7
Fig. 6.11
Fig. 6.12 Inferior and right ventricular infarction